Pharmacologically active strong acid solutions

ABSTRACT

A composition and therapeutic methods therefore for pharmacologically strong acid solutions comprising a mixture of strong and weak acids.

CLAIM OF PRIORITY

This application is related to provisional application Ser. No.60/282,026 filed on Apr. 6, 2001 based upon which priority is claimedpursuant to 35 U.S.C. § 119(e).

TECHNICAL FIELD

The present invention relates to compositions and methods of use of apharmacologically active acid solution in general and more particularlyconcerns the use of a low pH mixture of strong and weak acids whereinthe availability of hydronium ions in the mixture is highly controllableand which is non-corrosive to metals and innocuous to skin or otherorganic materials and is capable of topical or internal administration.

BACKGROUND OF THE INVENTION

The present invention relates to compositions of strong acid solutionsand therapeutic methods therefore.

More particularly, the invention relates to the use of a compositioncomprising a mixture of strong and weak acids, the final compositionacting as a buffer and having a pH of 1 or below.

Scientists are engaged in a constant battle to identify new therapeuticsfor treatment and prevention of disease in animals in general, andspecifically in humans. The search for active agents which are usefulagainst cancer is particularly acute. At present, a number of drugs areapproved for treatment of cancer. Recent approvals include Taxol®(paclitaxel), Cisplatin®, Taxotere® (docetaxel). None of these productsare active against all forms of cancer, all of them have significantside effects due to their cytotoxic effect on otherwise healthy cells.Due to the extreme toxicity of most cancer therapeutics, treating thecancer with such agents requires that the attending physician walk afine line between treating the cancer and killing the patient. Patientsexperience severe discomfort and a noted reduction in quality of lifedue to side effects of chemotherapy such as alopecia, general disruptionof the digestive system and feelings of malaise and general lack of wellbeing. Despite the power of modern cytotoxic agents, many cancers suchas glioblastoma are treated with only limited success using currentlyaccepted medical practices. As such, there is a long felt need foradditional cancer therapeutics. There is a particular need fortherapeutics that offer efficacy, low side effects and generally improvea patient's quality of life.

Acids have been used in pharmaceutical chemistry for decades, primarilyin the creation of acid addition salts of bases having therapeuticapplication. Lists of pharmacologically acceptable acids for thecreation of such salts are well known and are exemplified throughout thepatent literature. See U.S. Pat. No. 4,281,654 for a typical example.

The use of strong acids alone or in combination as a therapeutic isrelatively unknown to the scientific community. However, there are anumber of uses of acids as stabilizing agents. U.S. Pat. Nos. 5,733,888and 5,977,164, entitled Injectable Composition and StabilizedPharmaceutical Composition, issued to David Carver, et al., describe andclaim the use of various acids for stabilizing a pharmaceuticalformulation. Similarly, U.S. Pat. No. 5,504,102 also discloses the useof acids to stabilize a pharmaceutical composition.

The use of acid compositions alone is relatively unknown in theliterature. U.S. Pat. No. 5,552,389 describes and claims a method ofusing Phosphoric acid diesters to treat liver cancer. Santillo, M., etal., Inhibitors of Ras Farnesylation Revert the Increased Resistance toOxidative Stress in K-Ras Transformed NIH 3T3Cells, 229(3) Biochem.Biophys. Res. Commun. 739-45 (December 1996) discloses that phosphonicacid may suppress certain tumor genes. Kwun, K. B., et al., Treatment ofMetabolic Alkalosis with Intravenous Infusion of ConcentratedHydrochloric Acid, 146(3) Am J Surg 328-30 (September 1983) disclosesthe intravenous infusion of hydrochloric acid. Harguindey, S, et al.,Effects of Systemic Acidification of Mice with Sarcoma 180, 39(11)Cancer Res 4364-71 (November 1979) discloses that mineral acidificationof food decreased tumor growth and increased the rate of tumorregression.

Strong acid solutions having unique properties are disclosed in U.S.Pat. No. 4,675,120, issued to David J. Martucci, which describes andclaims an acid composition comprising water, hydrochloric acid,phosphoric acid, oxalic acid, citric acid and hydrofluoric acid usefulfor crude oil recovery.

Topical cosmetic or disinfectant uses of a strong acid compositionsimilar to that disclosed in U.S. Pat. No. 4,675,120 are disclosed inU.S. Pat. No. 5,512,200, which describes and claims a four acid corecomposition having very low pH comprised of a first and second inorganicacid and third and fourth organic acids. Inorganic acids disclosedinclude sulfuric, hydrochloric, hydrofluoric and phosphoric. Organicacids disclosed include oxalic and citric acids. The first and secondacids are present in a concentration between 5 and 20%. The third andfourth inorganic acids are present in an amount between 1 and 5% of thefinal composition. The above composition is said to be useful whenapplied topically as an antibacterial or antifungal agent.

To date there has been no apparent development of strong acid solutionsfor pharmaceutical use. Particularly, there has been no effort toexplore the potential internal uses for these unique agents.

SUMMARY OF THE INVENTION

In accordance with the present invention, herein disclosed is apharmaceutical composition comprising a mixture of four strong acids andtwo weak acids effective in treating a variety of medical conditions.

Numerous other advantages and features of the present invention willbecome readily apparent from the following description of the preferredembodiments of the invention, the accompanying examples, and theappended claims.

DESCRIPTION OF THE DRAWINGS

FIG. 1 shows the relationships between the hydronium ion donors andacceptors in the strong acid formulations of the present invention.

FIG. 2A is a photograph of a patient's ear with a tumor.

FIG. 2B is a photograph of patient's ear inf FIG. 2A after treatmentwith Formulation 1 of the present invention.

FIG. 3A is an echogram showing an enlarged ovary due to a tumor.

FIG. 3B is an echogram showing a normal ovary after the patient of FIG.3A was treated with Formulation 1 of the present invention.

FIG. 4 is a bone scan of a prostate cancer patient showing metastaticbone cancer.

FIG. 5 is a bone scan of the same patient in FIG. 4 after treatment withFormulation 1 of the present invention.

DETAILED DESCRIPTION OF THE INVENTION

The present invention discloses and teaches a new acid buffer solutionand its uses as a pharmacologically active agent. By following theteachings of the present invention, it is possible to create a bufferedsystem comprising an equilibrium mixture of strong acids conjugated withrelatively weaker acids. The system is obtained by respectivelycombining the strong acid with another strong acid and two relativelyweaker acids in the presence of water such that the conjugate bases ofthe relatively weaker acids serve as strong bases for controlling thehydronium ion availability or production from the strong acids. In thismanner, the characteristics of the strongest of the two strong acids canbe regulated.

It is therefore an object of the present invention to provide apharmacologically active buffered acid solution which exhibits low pHlevels coupled with highly controllable hydronium ion availability.

It is another object of the present invention to provide a low pHmixture of acids, which mixture is non-corrosive to metals used in themedical field to administer medication for example but not limitedintravenous needles and is innocuous to skin or other organic materials.

It is still another object of the present invention to provide a mixtureof two strong/weak acid pairs wherein the dissociation of the relativelyweaker acid in each acid pair supplies a conjugate base capable offunctioning as a strong base relative to the strong acid in each pair,thereby furnishing a means to control the hydronium ion availability orproduction from the strong acid.

It is yet another object of the invention to utilize the buffered strongacid compositions taught here in for the treatment or prevention ofdisease.

Another object of the present invention is to provide a pharmacologicalagent suitable for internal or external use.

It is a further object of the invention to treat cellular abnormalitiessuch as cancer.

It is a further object of the invention to reduce side effects normallyassociated with cancer therapeutics by administering the buffered strongacid solutions of the present invention.

It is yet another object of the invention to increase the life ofcatheters and other access methods to the circulatory system.

A. Formation of the Strong Acid Solutions

In a preferred embodiment of the present invention, a buffered solutionis made in two parts. A base strong acid solution is made from twostrong and two weak acids. Additional strong acids are added to the basestrong acid solution to create the buffered strong acid solution.

To create the base solution two strong and two weak acids are mixed toestablish a mechanism for controlling hydronium ion availability in theacids. A first balancing system is maintained between the conjugates ofone of the strong acids and the conjugates of a relatively weaker acid.The remaining pair of acids likewise forms a balancing system consistingof relatively strong and relatively weak acid conjugates. For presentpurposes, hydrochloric acid (HCl) and oxalic acid (H₂C₂O₄) are chosen asthe strong acids while phosphoric acid (H₃PO₄) and citric acid (H₈C₆O₇)are chosen as the weak acids relative to the strong acids.

From a comparative point of view, the application of Bronsted-Lowrytheory to the acid ionization reactions of hydrochloric, oxalic,phosphoric and citric acids will yield the following relationshipsbetween the conjugates of each acid: TABLE 1 Grade of Ionization Acid(α) Acid Conjugate Relationship HCl α = 1 Strong acid/weak conjugatebase H₃PO₄ α < 1 Weak acid/strong conjugate base H₂C₂O₄ α = 1 Strongacid/weak conjugate base H₈C₆O₇ α < 1 Weak acid/strong conjugate base

The relationship expressed in Table 1 can better be understood byobserving the actual ionization reactions of each acid within thecontext of the two strong/weak acid systems. Mixing the hydrochloric andphosphoric acids creates the first system of strong/weak acid pairs. Ina water environment, hydrochloric acid dissociates according to thefollowing equation:HCl+H₂O→Cl⁺H₃O⁺  Eq. 1

Similarly, in a water environment, phosphoric acid is dissociated intothree ionization states of decreasing strength as respectivelycharacterized by Equations 2-4:H₃PO₄+H₂O<=>H₂PO₄ ⁻+H₃O⁺  Eq. 2H₂PO₄ ⁻+H₂O<=>HPO₄ ⁻²+H₃O⁺  Eq. 3HPO₄ ⁻²+H₂O<=>PO₄ ⁻³+H₃O⁺  Eq. 4

The main source of hydronium ions in the mixture of hydrochloric andphosphoric acids is provided by the dissociation of the hydrochloricacid. Theoretically, it can be seen that the chlorine ions (Cl⁻) alsoproduced as a result of the ionization expressed in Equation 1 provide asalt for the hydrochloric acid. Given the strength of the hydrochloricacid, however, the chlorine ions as a practical matter cannotreassociate with hydronium ions at a rate fast enough to maintain astate of equilibrium during ionization. Hence, the production ofhydronium ions in pure hydrochloric acid remains unregulated. Incontrast, when phosphoric acid is added to the hydrochloric acid, theionization of phosphoric acid will serve as a partial regulator orcontroller of the hydronium availability in the hydrochloric/phosphoricacid mixture. Such regulation occurs because the first ionization stateof phosphoric acid, i.e., H₂ PO₄ ⁻, is present in relatively greatconcentration within the mixture of hydrochloric and phosphoric acids.While considered a semi-weak base per se, the first ionization state ofphosphoric acid acts as a relatively strong base in the presence of thestrong hydrochloric acid. Consequently, the first ionization constant ofphosphoric acid plays a primary role in capturing free hydronium ionspresent in the mixture of hydrochloric and phosphoric acids.

Despite the modifying effect of phosphoric acid on hydrochloric acid,the level of hydronium ion availability in a mixture of hydrochloric andphosphoric acids is too high to provide effective control over themixture. A second pair of strong and weak acids, e.g., oxalic and citricacids, must therefore be introduced to the mixture before actual controlcan be achieved. To this end, oxalic and citric acids are added to thehydrochloric/phosphoric mixture to provide a second strong/weak acidpair. The dissociation reactions of oxalic and citric acids are againanalyzed in a water environment, respectively yielding the followingequations:H₂C₂O₄+H₂O<=>HC₂O₄ ⁻+H₃O^(.+)  Eq. 5H₈C₆O₇+H₂O<=>H₇C₆O₇+H₃O^(.+)  Eq. 6

Although the hydrochloric acid serves as the primary source of hydroniumions in the two strong/weak pairs of acids, the oxalic acid is arelatively strong acid in its own right and thus constitutes a secondarysource of hydronium ions when added to the mixture of hydrochloric andphosphoric acids. The availability of the additional hydronium ions fromthe oxalic acid is quite important inasmuch as these additionalhydronium ions are responsible for the low pH of the full solution,i.e., the solution of hydrochloric, phosphoric, oxalic and citric acids.

The action of the citric acid in the full solution is also important.Adding oxalic acid alone to the hydrochloric and phosphoric acid mixturewould produce an over-abundance of hydronium ions, destroying thesought-after control of hydronium ion availability. The citric acid,however, is considered a weak acid, particularly in relation to theoxalic acid. As a result, the ionization state of the citric acid servesas a strong conjugate base for the oxalic acid. This strong conjugatebase in turn provides a secondary mechanism for controlling theavailability of hydronium ions from both the primary and secondaryhydronium ion sources, i.e., from both the hydrochloric and oxalicacids, in the full solution.

The entire mechanism for achieving control over hydronium ionavailability in the mixture of the present invention can now beunderstood. The first ionization state of phosphoric acid created bycombining the first strong/weak or hydrochloric/phosphoric acid pair andthe ionization state of citric acid created by combining the secondstrong/weak or oxalic/citric acid pair act in concert as relativelystrong bases to regulate the production of free hydronium ions withinthe solution. The first ionization state of phosphoric acid and theionization state of citric acid are both decreased by respectivelydrawing off free hydronium ions, thereby causing an increase in theconcentration of phosphoric acid and citric acid in the solution. Thislatter condition favors the ionization state of the hydrochloric andoxalic acids, in the process providing a strong source of hydronium ionsand allowing the ionization reactions expressed in Equations 2 and 6 toreach a state of equilibrium. The ionization of the oxalic acidadditionally produces oxalate ions which act as a strong base relativeto the hydrochloric acid, providing another means for capturinghydronium ions. As a net result, overall control of hydronium ionavailability in the full solution is readily attainable notwithstandingthe very low pH of the solution.

It should be noted in connection with the ionization reactions discussedabove that water plays a key role in the actual ionizing anddissociation mechanisms of the various acids in the present invention.Equations 1, 2, 5 and 6 all demonstrate that water functions as a strong“base” during the dissociation reactions, furnishing a carrier for thehydrogen ions released by the acids of the present invention. In thismanner, the various ionizations are greatly facilitated while theexchange of hydronium ions necessary to maintain equilibrium between thevarious dissociations and reassociations, and hence control overhydronium ion availability, is achieved. The key role of water in thepresent invention, and in particular the role of water in transportinghydronium ions between the reactants of Equations 1, 2, 5 and 6, isamply illustrated in FIG. 1.

The above acid solutions provide a stable environment that appears toregulate the otherwise corrosive effect of hydrofluoric acid (HF) andsulfuric acid (H₂SO₄) on tissues.

It has been discovered that new formulations of strong acids can beformulated for pharmaceutical use. A person of skill in the art willrecognize that the formulations described herein can be constructed of awide range of acids and concentrations by weight or volume. For example,the hydrochloric acid can range from 3-25 percent by weight, the oxalicacid from 0.1-10 percent by weight w/w, the phosphoric acid from 3-10percent by weight and the hydrofluoric acid from 1-30 percent by weight.Preferred is a composition in which the hydrochloric acid ranges from5-15 percent by weight, the oxalic acid ranges from 0.15-2 percent byweight, the phosphoric acid ranges from 2-7 percent by weight and thehydrofluoric acid ranges from 2-7 percent by weight. Most preferred is aformulation containing hydrochloric acid at 12 percent by weight, oxalicacid at 0.3 percent by weight, phosphoric acid at 6 percent by weight,sulfuric acid at 16 percent by weight and hydrofluoric acid at 5 percentby weight.

Formulation 1

First making a base solution from two strong and two weak acids to whichfurther strong and weak acids are added can manufacture a bufferedstrong acid solution suitable for internal use. Table 2 lists therelative concentrations of hydrochloric acid, phosphoric acid, oxalicacid, citric acid and water in the base solution used to make onepreferred embodiment of the present invention. TABLE 2 % Concentrationby Component Weight OxalicAcid 2% (H₂C₂O₄) Citric Acid 2% (H₈C₆O₇)Hydrochloric Acid 6% (HCl, d = 1.15 g/cc) Phosphoric Acid 6% (H₃PO₄, d =1.70 g/cc) Water 84% (H₂O)

In order to create 1000 ml of the base solution (Base Solution 1) fromwhich the buffer is created, the components listed in Table 2 arecombined in the following sequence:

(a) Oxalic acid (20 grams), which is generally in solid form, is addedto 200 ml water in a suitable reaction vessel at ambient temperature andis completely solubilized under continuous agitation;

(b) Following solubilization of the oxalic acid, citric acid (20 grams),which is generally in solid form, is added to the oxalic acid solutionobtained in (a) at ambient temperature with an additional 200 ml ofwater and is completely solubilized under continuous agitation;

(c) Following solubilization of the citric acid, the HCl (60 grams) isthen added to the solution of (b) while maintaining continuousagitation.

(d) Phosphoric acid (60 grams) is added to the solution obtained in (c)while maintaining continuous agitation.

(e) The resulting mixture obtained in (d) is agitated until allcomponents are dissolved. Water is added slowly until a final volume of1000 ml is obtained.

Adding the component of Table 3 to the Base Solution 1 creates thebuffered strong acid solution: TABLE 3 Component Density g/ml BaseSolution 1 N/A Sulfuric Acid 1.84 (H₂SO₄) Hydrochloric Acid 1.15 (HCl)Phosphoric Acid 1.70 (H₃PO₄) Hydrofluoric Acid 1.10 (HF)

Using the following steps creates 1000 ml of buffered strong acid.

-   -   (a) Add 150 ml of Base Solution 1 to a clean glass container.    -   (b) Slowly add 100 ml of sulfuric acid in small quantities, not        to exceed 10 ml, with continuous stirring. This is a highly        exothermic reaction which generates a very significant amount of        heat. Allow the sulfuric acid/Base Solution 1 mixture to cool to        ambient laboratory temperature.    -   (c) To the cool mixture from step (b), slowly add 30 ml        phosphoric acid with continuous stirring.    -   (d) To the cool mixture from step (c), slowly add 100 ml        hydrochloric acid with continuous agitation.    -   (e) Change the reaction vessel and stirring apparatus from glass        to plastic.    -   (f) To the mixture from Step (d), add 50 ml hydrofluoric acid        with continuous stirring.    -   (g) Add sufficient additional water to complete an aggregate        amount of 1000 ml of the buffered strong acid solution.

The buffered strong acid solution prepared according to the foregoingsequence of steps is characteristically modified in the sense that thesolution has a pH of less than 1, has strong buffering capacity and iscompletely stable at ambient temperatures between 0 and 70° C. andnormal light. The buffered strong acid solution is non-corrosive andnon-toxic, e.g., innocuous to skin. It is surprising that the HFcontained in the buffered strong acid solution of present invention doesnot burn the skin. The exact manner by which the solution avoids damageto the skin has not yet been determined.

Although exhibiting the beneficial characteristics discussed above, thesolution of Formulation 1 maintains a high level of acidizing potential.That is, the pH level of the solution is quite low, generally on theorder of less than 1.

Formulation 2

Altering the concentrations of the acids can create an alternativeembodiment of a strong acid solution having medical use, but verylimited buffering capacity. Similar to Formulation 1, Formulation 2 iscreated from a base of the four acids set forth in Table 4, which liststhe relative concentrations of hydrochloric acid, phosphoric acid,oxalic acid, citric acid and water in Base Solution. TABLE 4 %Concentration Component By Weight Oxalic Acid 3% (H₂CO₄) Citric Acid 3%(H₈C₆O₇) Hydrochloric Acid 5% (HCl, d = 1.15 g/cc) Phosphoric Acid 5%(H₃PO₄, d = 1.70 g/cc) Water 84% (H₂O)

In order to create 1000 ml of the base solution (Base Solution 2) fromwhich Formulation 2 is created, the components listed in Table 4 arecombined in the following sequence:

-   -   (a) Oxalic acid, which is generally in solid form, is added to        200 ml water in a suitable reaction vessel at ambient        temperature and is completely solubilized under continuous        agitation;    -   (b) Following solubilization of the oxalic acid, citric acid,        which is generally in solid form, is added to the oxalic acid        solution of (a) at ambient temperature and is completely        solubilized under continuous agitation;    -   (c) Following solubilization of the citric acid, the        hydrochloric is added to the solution obtained in step (b),        while maintaining continuous agitation.    -   (d) Phosphoric acid is added to the solution obtained in step        (c), while maintaining continuous agitation.    -   (e) Sufficient water is added to the solution obtained in step        (d), complete an aggregate amount of 1000 ml of this low pH        solution (Base Solution 2).    -   (f) The resulting mixture obtained in step (e) is agitated until        all components are fully dissolved.

The topical strong acid solution (Formulation 2) is created by mixingthe components of Table 5: TABLE 5 % Concentration Component By VolumeBase Solution 2 40 Sulfuric Acid 20 (H₂SO_(4,) d = 1.84 g/cc)Hydrochloric Acid 10 (HCl, d = 1.15 g/cc) Phosphoric Acid 10 (H₃PO₄, d =1.70 g/cc) Hydrofluoric 15 (HF, d = 1.10 g/cc) Glycerin 5 (d = 1/24g/cc)

1000 ml of topical strong acid is created by using the following steps:

-   -   (a) Add 400 ml of Base Solution 2 to a clean glass container.    -   (b) Slowly add 200 ml of sulfuric acid to the Base Solution 2        with continuous stirring. This is a highly exothermic reaction        which generates a very significant amount of heat. Allow the        sulfuric acid/base Solution 2 mixture to cool to ambient        laboratory temperature.    -   (c) To the cool mixture obtained in step (b), slowly add 100 ml        phosphoric acid with continuous stirring.    -   (d) To the mixture obtained in step (c), slowly add 100 ml of        HCl with continuous agitation.    -   (e) Change the reaction vessel and stirring apparatus from glass        to plastic.    -   (f) To the mixture obtained in step (d), slowly add 150 ml HF        with continuous stirring.    -   (g) To the mixture from step (f), add 50 ml of glycerin.

The strong acid solution prepared according to the foregoing sequence ofsteps is characteristically modified in the sense that the solution hasa very low pH, and is completely stable at ambient temperatures between0 and 70° C. and normal light. The strong acid solution is non-corrosiveand non-toxic, e.g., innocuous to skin. It is surprising that the HFcontained in the strong acid solution of Formulation 2 does not burn theskin. The exact manner by which the solution avoids damage to the skinhas not yet been determined.

B. Pharmaceutical Uses and Administration of Strong Acid Solutions

The buffered strong acid solution (Formulation 1) may be administered inany medically accepted manner, except that solid dosages forms may bedifficult to produce due to the pH. These compounds of the presentinvention are administered in a pharmaceutical composition and mayinclude suitable excipients, the composition being useful in treatingdisease. Method of formulating compositions for an intendedpharmaceutical use are well known in the art. A generally recognizedcompendium of such methods and ingredients is Remington's PharmaceuticalSciences by E. W. Martin (Mark Publ. Co., 15 Ed., 1975), which is herebyincorporated by reference herein.

Methods of administration include but are not limited to: topical, oral,intravenous (IV), intramuscularly, intraperitoneal, rectal,intraurethral, intravesical, and intravaginal. The most preferredmethods for Formulation 1 are oral or IV, either peripheral orsubclavian/central. Formulation 2 can only be administered topically andinternal administration of Formulation 2 may be lethal.

When administering the buffered strong acid solution orally, patientsmay be given between 5 and 1000 drops of Formulation 1 per day. Thebuffered strong acid solution Formulation 1 can be administered directlyto a patient, however, the preferred patient dosage is from 10-200 dropsper day diluted in 100-1000 ml. of liquid, preferably juices preparedfrom fresh fruit, not from concentrate. Most preferred is 20-30 drops in200 ml of liquid. Citrus juices or other acid containing beveragesshould be avoided due to increased potential for irritation of thedigestive tract and possible reaction with the buffered strong acids ofthis invention. Milk and dairy based beverages should be avoided becausethe acids will curdle the milk.

In a preferred form of administration, patients are initially titratedfrom a dose of 20-30 drops in 200 cc of Formulation 1, diluted innon-citrus fruit juices, given for 1-2 days and the patient observed forany adverse reaction. If no reaction is observed, the dose can beescalated to 20 drops 3 times a day and adjusted upward, as tolerated byan individual patient. A suggested daily dose after titration is 100-150drops per day, however, some patients may not tolerate more than 70drops per day. It is preferred that the daily dosage be divided into20-30 drop quantities and administered at appropriately spaced intervalsthroughout the day. Formulation 1 should generally be added to a minimumof 200 ml of liquid, 20 drops are equivalent to 1 cc or 1 ml of fluid.

It is important that this product not be taken on an empty stomach.While there are generally no side effects from ingesting the bufferedacid composition as described above, the added acids may cause heartburnand/or acid indigestion. At the discretion of the attending physician,precautions should be taken when giving this product orally to patientswho have a history of digestive tract problems or who are undergoingchemotherapy. Recommended precautions comprise a premedication regimencomprising H₂ blockers, digestive tract anti-inflammatories and/or ananti-emetic. The premedication regimen should be administered one halfto one hour before administration of Formulation 1 in accordance withthe product labeling each agent administered.

Due to the difficulties of administration and the apparentbioavailablity of the buffered strong acids of Formulation 1 whenadministered orally, IV administration is less preferred except when thepatient requires higher doses than may be tolerable through oraladministration. In such instances, the buffered strong acid solutionstaught herein can be administered through any suitable vein. Mostpreferred for the highest doses and for frequent dosing isadministration through a surgically implanted subclavial catheter. Whenadministering the buffered strong acid solution IV, it should be dilutedin a suitable IV fluid such as glucose, dextrose or saline. In suchinstances 8 ml of buffered strong acid may be diluted in 250-1000 ml ofinfusion fluids. It is preferred to administer 2 ml of the Formulation 1in approximately 250 ml of infusion fluids. The preferred rate ofinfusion is 20-40 drops per minute at which rate it will takeapproximately 4-8 hours to administer the solution. Higher dosages arealso possible, for example, 100 drops administered in 500 ml of fluid.However, with higher concentrations, the infusion rate should be reducedto approximately 25 drops per minute.

When administering buffered strong acid solutions IV, peripherally, suchas through a vein in the arm or leg, it is preferable to use a very fineand long needle and dose the patient every other day or one week e.g.,Monday, Wednesday and Friday, followed by a one week rest and thenresume an every other day infusion schedule. Because there appears to beno dose limiting toxicity when administered as described herein, thereis no limit on how long a patient may be dosed with the buffered strongacid solutions of Formulation 1. If reactions occur in the veins,topical application of an anti-inflammatory may help.

It should be readily apparent to one of skill in the art thatcombinations of routes of administration such as but not limited to oraland IV administration (either peripheral or sub-clavian) are possibleand may be desirable when seeking to administer higher or more frequentdoses to a patient.

Intra-muscular administration is possible but may be less preferredbecause of the formation of lesions. Similarly, intra-peritonealadministration is also possible, but may not be desirable due to theneed to administer in a hospital setting.

The formulations disclosed in this patent are generally safe foradministration when used as directed herein. However, certain patientswill require extra care prior to administration of the pharmaceuticalformulations disclosed in this patent. For example, in patients withhigh blood levels of creatinine and urea which may be indicative ofkidney failure, it is advisable to bring these values within normalrange prior to treatment with the formulations disclosed herein.Similarly, it is also desirable to correct conditions of low bloodpressure, below 90/60, prior to treatment with the internal formulationsdisclosed in this application.

Formulation 1 does not affect blood pH when administered in accordancewith the methods described in this patent. It is generally known thatwhen an acid is added to extra-cellular fluid, it is rapidly absorbed bythe carbonic acid/bicarbonate buffer which is the primary regulator ofH₃O⁺ levels in living systems. The buffered acid formulations disclosedherein contain closely regulated levels of H₃O⁺. As such the bufferingsystems in living beings appears to be able to absorb any additionalamounts introduced through the buffered strong acids. The hydrofluoricacid, which is the primary free acid in the formulation, contributeslittle H₃O⁺. It is postulated but unproven that hydrofluoric acid mayform important complexes with proteins or other buffering agents leadingto the surprising activity of buffered acid solutions. The mechanism ofaction of the present formulation is a matter for further research andinvestigation.

At present, the formulations disclosed in this application whenadministered as described herein have shown unique activity against anumber of medical conditions.

It has been discovered that subclavial ports can be left in for extendedperiods of time. Normally, such ports last 7-10 days before their use bereplaced, due to infection. Patient's administered the formulationsdisclosed herein have shown no sign of infection around the port forperiods as long as 95 days. It is believed that this effect is due tothe activity of Formula 1 against most known bacterial, viral and fungalinfections.

Antiviral activity has been demonstrated in vitro and in a clinicalsetting. Both Formulation 1 and 2 disclosed herein have demonstratedactivity in patients against the Human Papilloma Virus (HPV), Poliovirus and Encephalitis virus.

Data have shown that the formulations disclosed herein are selectiveneoplastic agents that appear to have no impact on normal healthy cells.The compositions only attack neoplastic cells. Animal studiesdemonstrated the destruction of chromatin in neoplastic cells whilenormal cells remained unaffected. Tumors are affected without affectingnormal tissues.

Not only are the strong acid compositions disclosed herein effective intreating known tumors in patients, experiments have shown that thestrong acid solutions prevent the formation of tumors. The presentinvention also appears to prevent or treat micro metastasis.

Very surprising is the observation that the buffered strong acidformulations are effective in treating brain tumors. It is postulatedthat unlike most chemotherapeutic agents, the active moiety of thebuffered strong acid formulation is able to cross the blood brainbarrier. This is evidenced by tumor shrinkage and by a reduction ofpressure in the cranial cavity.

Administration of Formulations 1 and 2 has shown anti-mycotic activityagainst all known fungi.

Cancer patients receiving the buffered strong acid of Formulation 1disclosed herein are able to stop taking pain medication. For reasonsunknown, the strong acid buffered solutions serve to alleviate pain incancer patients.

The buffered strong acids have shown significant reductions in tumoralmarkers. As shown in the examples, reductions to normal levels have beenobserved in TM 15-3 in breast cancer and PSA in prostate and also inalkaline phosphatase levels in patients with bone cancer metastasis.

When administered as described herein, the buffered strong acidformulations have been shown to generally improve the quality of lifefor cancer patients. They feel stronger in a couple of days afterinitiating treatment. Significantly, they experience a return ofappetite and normal sleeping patterns. Patients immobilized due toexhaustion or pain often regain mobility.

The buffered strong acid solutions also appear to have significantbenefit on the circulatory system. A significant lowering of bloodpressure has been observed in patients receiving buffered strong acidswhere prescription medication failed to have effect. The buffered strongacids can be used either alone or in conjunction with prescriptionmedication.

Table 6 lists the acceptable ranges of concentration for each of theacids added to the Formulations 1 and 2. TABLE 6 Component Range (%volume) Hydrofluoric Acid 1-40% Hydrochloric Acid 2-30% Sulfuric Acid2-30% Phosphoric Acid 1-30%

The strong acid solutions of Formulation 1 and 2 can be used for thetreatment of a wide range of diseases. Formulation 1 is appropriate forinternal administration to treat cancer, high blood pressure, infectiousdisease of viral, bacterial or fungal origin including human Papillomavirus and HIV. Formulation 1 when given intravenously extends the lifeof catheters and other venous access ports. Formulation 2 is appropriatefor topical administration to treat melanoma and infections of the skin.Specific examples showing the use of the strong acid compositions ofFormulations 1 and 2 are set forth below.

EXAMPLE 1 Melanoma Cells

Formulation 1 was diluted with saline solution in concentrations of 1:10to 1:100,000 and plated in petri dishes containing growth media andmelanoma cell line murine B-16 from Jackson Hospital mice. Dilutions of1:10 to 1:100,000 of Formulation 1 were plated. The results are shown inTable 7. TABLE 7 Dilution # Of Surviving Cells Control 100% 1:10 0 1:1000 1:1,000 0 1:10,000 0 1:100,000 0

These results show that the Formulation 1 is a powerful cytotoxic agent

EXAMPLE 2 Bacteria

Formulation 1 was tested for anti-bacterial activity using Kirby-Bauermethods. staphylococcus aureus, Escheria coli, Klebiella pneumoniae,Pseudomonas aerigonosa, Acinebacter Baumannii, Enteroccoccus, spp. weregrown in soy media at 35° C. for 16-18 hours and diluted with saline to0.5 McFarland and plated on Mueller-Hinkle plates. 0.1 ml of Formulation1 was added to each plate and dried. Each plate was incubated 18-21hours at 35° C. All bacteria present were destroyed.

EXAMPLE 3 Encephalitis

The effects of Formulation 1 on encephalitis were tested in kidneyderived Green Monkey VERO cells.

Protocol

VERO cells having a normal life span of 7-10 days were grown in EagleMEM with 10% Bovine Fetal Serum and 1% antibiotic/anti-mycotic agent in25 cm3 cultures. Testing for activity of Formulation 1 againstencephalitis was performed using the following controls and experimentalplates.

Negative Control comprised of a plated monolayer of VERO cells on themaintenance medium containing 2% Bovine Fetal Serum.

Toxicity Control comprised of a plated monolayer of VERO cells on themaintenance medium containing 2% Bovine Fetal Serum with 600 μl ofundiluted Formulation 1 added.

Positive Control comprised of a plated monolayer of VERO cells on themaintenance medium containing 2% Bovine Fetal Serum and inoculated with600 μl Goajira version of encephalitis virus.

Experiment 1 comprised of a plated monolayer of VERO cells on themaintenance medium containing 2% Bovine Fetal Serum and inoculated with600 μl Goajira version of encephalitis virus with 600 μl of undilutedFormulation 1 added to the plate.

Experiment 2 comprised of a plated monolayer of VERO cells on themaintenance medium containing 2% Bovine Fetal Serum and inoculated with600 μl Goajira version of encephalitis virus with 600 μl of Formulation1 diluted 1:2 with water added to the plate.

Experiment 3 comprised of a plated monolayer of VERO cells on themaintenance medium containing 2% Bovine Fetal Serum and inoculated with600 μl Goajira version of encephalitis virus with 600 μl of Formulation1 diluted 1:10 with water added to the plate.

All plates were initially incubated for 1 hour at 37° C. in 5% CO₂ toallow viral adsorption. Formulation 1 was added to those platesidentified above and the cultures were maintained at 37° C. andobserved.

Results and Observations

Those plates receiving Formulation 1 turned a uniform yellow color assoon as Formulation 1 was added.

On the second day post infection, the cytotoxic effects of the virus wasevident in 75% of the monolayer of the positive control. In the negativecontrol, the monolayer remained confluent and demonstrated nomorphological changes to the cells. The experimental plates 1, 2 and 3which contained Formulation 1 also remained confluent and demonstratedno morphological changes to the cells.

On the 5th day post infection, the virus destroyed all the cells in thepositive control. The cells of the negative control remained confluentbut showed expected signs of aging. The cells of the experimental plates1, 2 and 3 remained a confluent monolayer and showed no signs of aging.

Two months post infection, the cells of the experimental plates 1, 2 and3 remained alive and demonstrated no signs of aging.

Three months post infection, the laboratory where the experiments wereconducted suffered a long term power outage. All of the ongoingexperiments in the laboratory were destroyed except for the experimentalplates containing Formulation 1.

EXAMPLE 4 Polio Virus

Formulation 1 was tested against poliovirus in African Monkey derivedMA104 cells.

Protocol

MA 104 cells having a normal life span of 7-10 days were grown in EagleMEM with 10% Bovine Fetal Serum and 1% antibiotic/antimycotic agent in25 cm3 cultures. Testing for activity of Formulation 1 againstencephalitis was performed using the following controls and experimentalplates.

Negative Control comprised of a plated monolayer of MA104 cells on themaintenance medium containing 2% Bovine Fetal Serum.

Toxicity Control comprised of a plated monolayer of MA104 cells on themaintenance medium containing 2% Bovine Fetal Serum with 600 μl ofundiluted Formulation 1 added.

Positive Control comprised of a plated monolayer of MA104 cells on themaintenance medium containing 2% Bovine Fetal Serum and inoculated with600 μl poliovirus.

Experiment 1 comprised of a plated monolayer of MA104 cells on themaintenance medium containing 2% Bovine Fetal Serum and inoculated withpolio virus with 600 μl of undiluted Formulation 1 added to the plate.

Experiment 2 comprised of a plated monolayer of MA104 cells on themaintenance medium containing 2% Bovine Fetal Serum and inoculated withpolio virus with 600 μl of Formulation 1 diluted 1:2 with water added tothe plate.

Experiment 3 comprised of a plated monolayer of MA104 cells on themaintenance medium containing 2% Bovine Fetal Serum and inoculated withpolio virus with 600 μl of Formulation 1 diluted 1:10 with water addedto the plate.

All plates were initially incubated for 2 hours at 37° C. in 5% CO₂ toallow viral adsorption. Formulation 1 was added to those platesidentified above and the cultures were maintained at 37° C. andobserved.

Results and Observations

Those plates receiving Formulation 1 turned a uniform yellow color assoon as Formulation 1 was added.

On the third day post infection, the cytotoxic effects of the poliovirus was evident in 50% of the monolayer of the positive control. Inthe negative control, the monolayer remained confluent and demonstratedno morphological changes to the cells or signs of aging. Theexperimental plates 1, 2 and 3 which contained Formulation 1 alsoremained confluent and demonstrated no morphological changes to thecells or signs of aging.

On the 5th day post infection, the virus destroyed 100% of the cells inthe positive control. The cells of the negative control remainedconfluent but showed expected signs of aging. The cells of theexperimental plates 1, 2 and 3 remained a confluent monolayer and showedno signs of aging.

Two months post infection, the cells of the experimental plates 1, 2 and3 remained alive and demonstrated no signs of aging.

Three months post infection, the laboratory where the experiments wereconducted suffered a long term power outage. All of the ongoingexperiments in the laboratory were destroyed except for the experimentalplates containing Formulation 1.

EXAMPLE 7 Venereal Tumors

A female canine was diagnosed with nodular vaginal tumor. The nodule wasa soft homogenous tumor of 1.5 cm in diameter. Formulation 2 wastopically applied to the surface of the tumor daily for 7 days. By the7^(th) day, the tumor had shrunk from a round nodule to a 1.5 cm plaque.There was no effect to surrounding residual cells. Tissues were analyzedby microscopy and determined to still be neoplastic. Formulation 2 wasdetermined to have significant anti-tumor activity, even though someneoplastic cells remained. It was noted that Formulation 2 had no effecton healthy tissues.

EXAMPLE 8 Lymphoma

A canine great dane, age 7 years was disguised with cutaneous lymphomaand lymphatic sarcoma. Subject had open and oozing ulcerations on theskin. Subject was treated with 25 cc of Formulation 1 subcutaneously and3 ml of a 1:10 cc Formulation 1 given intramuscularly. Formulation 1 wasadministered every other day for one (1) month. During treatment, theulcerations dried up. Subject died nine (9) days post treatment ofcauses unrelated to treatment.

EXAMPLE 9 Venereal Tumors

A female Doberman, aged 6 years, was diagnosed with tumors of the vulvaand vagina. The vaginal tumor was the size of a small lemon andexhibited persistent bleeding. The tumor was surgically removed and thesubject treated with chemotherapy. The tumor returned in 30 days withhemorrhaging. Subject was treated with Formulation 1 topically for two(2) days, during which time the hemorrhaging continued. After two (2)days, 0.25 ml of Formulation 1 was injected into the tumor inconjunction with topical administration. The dosing regimen was repeatedevery other day for 20 days, upon which time, the tumor disappeared. Aparenchymal tumor of the mammary gland of the same subject was injectedwith 0.25 ml of Formulation 1. This tumor disappeared in 48 hours,leaving an opening in the site, where injected.

In a separate experiment, 3 male, 3 female and 3 fixed canines werediagnosed with venereal tumors. Formulation 2 was applied topically tothe tumors once a day for 15 days. Formulation 1 was administered IV 5cc daily in 11.5 cc of fluid suitable for IV administration. Clinically,all bleeding tumors stopped bleeding and a reduction was noted in alltumors. In all instances of IV administration, there was no observablechange in the subjects hematology, urinalysis or blood chemistry.However, if not administered directly to a vein, there were signs ofedema and localized necrosis. Only one (1) subject had a tumor returnwithin 30 days of cessation of treatment.

EXAMPLE 10 Head and Neck Cancer

A 46 year old male patient diagnosed with a 2 cm carcinoma of the tonguewas unsuccessfully treated with chemotherapy and radiation. Patient wasdiagnosed with a possible cancerous tumor in the tongue and underwent abiopsy which confirmed the tumor was cancerous. Three months laterpatient underwent surgery to remove the tumor. A biopsy of the removedtissue confirmed that it was cancerous. Following the surgery patientunderwent 6 weeks of chemotherapy comprising 5-Fluorouracil,carboplatin, interferon and retinoids. Two weeks following thechemotherapy, the patient received radiation therapy and was treatedwith Vesanoid® (tretinoin) for five months post radiation. The patientcontinued to have high tumoral markers, lost weight and felt weak andtired. Patient's tumor markers were Ki67-2+; PCNA-3+; P53-3+. (2 isconsidered moderate and 3 is considered elevated).

One year post diagnosis, patient start taking twenty (20) drops ofFormulation 1 diluted in 250 ml of fruit juice was administered three(3) times per day for 90 days. Tests taken fifteen months post diagnosisshowed that the patient's, T and B cells were back within normal rangebut that there was a slightly elevated CD4 count and suppressor cells.The patient's CD4/CD8 ratio was substantially reduced. Patient rapidlyregained vitality and today shows no signs of cancer except for anelevated CD4/CD8 count, which the attending physician considers normalfor this patient.

EXAMPLE 11 Head and Neck Cancer

A female patient age 5 was diagnosed with a Granulomatoid lesion in theright ear (Hystiocitosis X) following a biopsy. At the time of diagnosisthe tumor completely obstructed the ear canal of the right ear and wasbleeding. A picture of the tumor is shown in FIG. 2A. Three weeks laterthe patient initiated oral treatment with Formulation 1 at a dose of 20drops 3 times a day. When treatment was initiated the patient receivedan abdominal echogram which identified a bent gallbladder and a slightlyenlarged pancreas but with no other abnormalities. The following week acranial X-ray was taken showing perforations in the cranium. A bone scanperformed six weeks post diagnosis identified an abnormal accumulationof the radiotracer in the head, close to the right ear, confirming theoriginal diagnosis. At this time the patient experienced a bloodysecretion from her right ear, but was otherwise doing well the followingweek, a cytogenetical study is performed for a granuloma eosinofilicustumor. In 94% of the metaphase cells a normal complement was observed.However, two karyotypes were identified with close complement to thetetraploidia with five copies of the chromosomes 7, 14, 20 and 21; threecopies of chromosomes 17, 18 and 19, and four copies of the otherautosome chromosomes. Conclusions: There has not been established aclear correlation with the presence of cytogenetic alterations in thepatients with granuloma eosinofilicus. However, a karyotype tretraploidehides the forecast in hematological malignancies.

Four months post diagnosis the patient's mother indicates that herhealth is improving and that the patient has resumed normal sleep habitsand had a good appetite. Urination was normal although patient sufferedslight constipation. The secretions from the ear had ceased and anymalodors had ceased. Examination by an otolaryngologist shows that thetumor had shrunk to a circle of approximately 2¼ cm diameter, andsuggested to continue treatment with Formulation 1. A CAT scan taken atfour and a half months post diagnosis does not identify any lesions. Atsix months post diagnosis the tumor is undetectable. At eight monthspost diagnosis, the otolaryngologist confirms total disappearance oftumor from the ear. One year post diagnosis, the patient was consideredto be in normal health and free of any tumor. FIG. 2B shows the rightear of the patient after treatment with Formulation 1.

EXAMPLE 12 Breast Cancer

A 34 year old female patient diagnosed with breast cancer underwent amastectomy for the tumor. A biopsy on the tissue confirmed that thetumor was an infiltrating carcinoma of the breast. Four months after themastectomy, the patient was diagnosed via CAT scan with a neoplasticmetastasis from the breast cancer in her hip. This diagnosis wasconfirmed two months later through an MRI. The tumors were surgicallyremoved and the patient underwent 8 rounds of therapy with Taxol® withconcominant treatment with Vesanoid®. At 31 months after diagnosis, andfollowing the Taxol therapy, this patient had high tumor markers. CA15.3 markers were 71.73 and CA 125 was 40.50. At this time patient begantaking 80 drops per day of Formulation 1. Four weeks after startingtreatment with Formulation 1, this dose was increased to 120 drops perday. The Ca 15.3 maker and the Alkaline phosphatase (AP) level began todecrease immediately following the increase in dosage. For 10 months,the patient has only been treated with Formulation 1, 120 drops per day.Eleven months after initiating treatment with Formulation 1, all of thepatient's tumor markers were normal and the alkaline phosphatase levelcontinued to decrease.

EXAMPLE 13 Breast Cancer

Female patient, aged 78, was diagnosed with a tumor in her left breast.Tumor continued to increase in size over a 2 year period followingdiagnosis. During that time the patient had lost weight and looked pale.A mammography and biopsy showed a 2.5 cm nodular lesion in the breastwith a diagnosis of lobular infiltrating carcinoma. Due to her advancedage, surgical intervention was inadvisable. Patient began takingFormulation 1 orally, 10 drops per day gradually increasing the dose to50 drops a day for 2 months. Patient had no observable side effects. Twomonths after initiating oral treatment, patient started IV treatment of0.5 cc per day of Formulation 1 in glucose every other day for 1 month.Following intravenous administration the patient experienced somephlebitis and edema in her arm. During the month of IV treatment, thepatient's skin color improved and she gained 2 kgs. of weight. After onemonth of IV therapy, the patient resumed oral treatment of Formulation 1at a dose of 50-60 drops a day for 1 year and 4 months. Anothermammography was performed and showed a 4 cm mass but surprisingly showedthat the axilar lymphs region was free of malignancy. Today the patientcontinues oral therapy using Formulation 1 and is alive and in goodhealth.

EXAMPLE 14 Breast Cancer

Female patient, aged 37 under went a biopsy and was diagnosed withDuctal infiltrating Carcinoma in the left breast. 16 region aladenopathies were identified and surgically removed, of which 10 weremalignant. The patient was treated by an oncologist with 6 cycles of thefollowing drugs: Farmarubicin, Taxol, Daxorubicin, 5-FU, Citoxan,Ethyol, Cardioxane, Zofran, and Decadron among others. Patient wastreated with: 2 cycles of chemotherapy, then 30 sessions of radiotherapyin the affected area and then the remaining 4 cycles of chemotherapy.Following chemotherapy, patient was placed on Evista and Raloxifen. Oneyear after ending chemotherapy, patient suffered nausea, almostpermanent headaches and a sensation of pressure in her head and wasdiagnosed with a brain tumor. At that time patient was depressed andanxious but suffered no memory or language problems or problems withmobility. Patient suffered from paresis in left side of face and in herleft limb.

A CAT scan performed at that time shows the existence of a cystic mass6.5 cm×6.5 cm, with thick capsule in left parietal side compatible witha possible metastatic lesion (melanoma, coriocarcinoma), glioblastomamultiforme or cerebral abscess. With an antecedent of adenocarcinoma isvery possible that is that one. MRI ratified the observation made in theCAT. Treating physicians were surprised that with the existence of alarge lesion that there was not a big edema.

The patient underwent surgery one month after diagnosis of the braintumor and, under general anesthesia, a left parietal craniotomy wasperformed identifying a lesion that was infiltrating the dura mater. Thelesion was detached easily. The lesion was of cystic nature and 6 to 8cc of dark amber color liquid were extracted. The capsule was of variedthickness and was very differentiated from the rest of the cerebralparenquima, with almost no vascularization. The capsule was whitish andgranular showing evidence of a malignant tumor. The resection wascomplete and the dura mater was scraped and cauterized with nomacroscopic evidence of the tumor.

A biopsy of the frozen tumor confirmed a diagnosis of metastaticadenocarcinoma in the left parietal side of the brain. Post surgery,patient underwent 10 sessions of radiotherapy of 300 CGY each for atotal of 3000 CGY. She was instructed to take Medrol (a corticosteroid)and Neubion (a B complex vitamin) for 2 weeks followed by phenobarbitalfor 6 months. After 2 months post surgery the patient had not regainedher vigor. At that time patient initiated treatment using 30 drops ofFormulation 1 orally per day, increasing to 120 drops per day, which iscontinued to this day. Eight months post surgery, the patient visited anOncologist at Jackson Memorial Hospital in Miami, who found her to be invery good state of health after performing a set of tests. During a oneyear period the patient has taken a total of 620 cc of Formulation 1orally.

EXAMPLE 15 Cancer of the Digestive Tract

A 53 year old male patient was diagnosed with epidermoid carcinoma ofbig cells in the anal region at which time the patient was hospitalizedand treated with 3 cycles of 5FU and Leucovorin and 25 cycles ofradiation therapy. The tumor did not respond to therapy and causedproblems with urination and defecation. One month post diagnosis thepatient was advised his cancer was terminal. Two months post diagnosis,the patient initiated treatment with Formulation 1 at a dose of 140drops a day (7 cc) and continued treatment for 8 months. At eightmonths, the dosage was reduced to 100 drops per day, which dose has beenmaintained until the filing of this application. The patient'shemoglobin value rose from 5 to 11 during the treatment period and thepatient regained his appetite and gained weight. All difficulties withurination, defecation an rectal bleeding disappeared. The patientreceived no other treatment for his cancer during the time he wasadministered Formulation 1.

EXAMPLE 16 Condylomata Acuminata

Condylomata Acuminata are genital warts caused by certain humanpapillomaviruses (HPV). A study was performed by a dermatologist on 20male patients between the age of 20 and 25 years of age. Location of thecondilomas was on the penis glade and on the inside of the skin of thepenis. Formulation 2 was applied full strength with a Q-tip, allowingthe drug to work for the next 24 hours. Afterwards the affected regionwas washed with soap and water and the regiment repeated every sevendays for 3-4 weeks. Following treatment; 5 Cases healed with oneapplication, 8 Cases healed with two applications, and 5 Cases healedwith three applications. Two Cases did not return to doctor'sappointment after the first treatment.

EXAMPLE 17 Multifocal Basal Cellular Cancer in the Face

Female patient, age 11, was diagnosed following a biopsy with multifocalbasal cellular cancer in the face. The tumors were removed surgically ontwo occasions following, which the tumors immediately returned andspread. Formulation 2 was administered full strength every other day forfive applications. The tumors disappeared and have not returned.

EXAMPLE 18 Malignant Melanoma in the Left Leg

Female patient, aged 67, underwent surgery twice to remove melanoma fromher left leg. Patient was symptom free for five years when inguinallymphs in the left leg showed increased in volume. Patient was treateddaily with full strength Formulation 2 topically with a cotton swab fora total of six treatments in the affected area. Following treatment, thelymphs reduced volume until they almost disappeared. The patient howeverdied due to recidivisms with metastasis in the pulmonary and liverlymphs.

EXAMPLE 19 Endodermic Papilloma in Left Arm

Patient suffered from Endodermic papilloma in the left arm. Tumor wasresistant to all treatment for a period of ten years. Formulation 2 wasapplied full strength every half hour the same day for two days,followed by administration every other day for two weeks. Followingtreatment with Formulation 2, the disease has disappeared and has notreturned

EXAMPLE 20 Brain Cancer Medulloblastoma

A 27 year old male patient complaining of headaches was diagnosed with amedulloblastoma following a CAT scan and confirmed the following weekthrough an MRI to be a medulloblastoma in the 4th ventricle withhydrocephalia and a possibility of glioma. The patient was onlyadministered analgesics for the headaches. Six months following theinitial diagnosis, the tumor had grown to 40×35×32 mm with obstructionof the 4th ventricle. During the 10th month after diagnosis patient wasgiven 3000 CGY of radiation. Eleven months post diagnosis, a drain valvewas installed to reduce the pressure and an additional 200CGY ofradiation administered. Patient continued to suffer from severeheadaches, difficulty in walking, nausea, vomiting and blurred vision inhis right eye. At approximately one year post diagnosis, an MRI confirmsa 3.2×2.7×2.1 tumor. Patient initiated oral treatment with Formulation 1at 30 drops per day increased to 140 drops per day diluted in juice andsoups. After one month of treatment the patient began to showsignificant changes in the pathology of the tumor. The headacheslessened in severity and disappeared within two months of initiation oftreatment with Formulation 1. The patient also regained his equilibriumand his vision returned to normal. By the end of the third month oftreatment, the patient had resumed all normal daily activities. Afterapproximately four months of treatment with Formulation 1, the patientunderwent a CAT scan which indicated “no evidence of apparentintracerebral lesions.” This was subsequently confirmed by an MRI.

EXAMPLE 21 Brain Cancer (Glioblastoma Multiforme)

A 38 year old male presented with a convulsive crisis with noticeableweakness in his left arm and leg. CAT scan and MRI confirm a tumor inthe right frontal lobe of the brain. Two weeks following diagnosis, thetumor is surgically removed and diagnosed as gemistocystic astrocitoma.A week later the patient was discharged and received radiotherapy overthe following three months. Five months after the initial diagnosis, thepatient suffered a new convulsive crisis and was readmitted to thehospital. A MRI taken at the time identified an infiltrating lesionaffecting the right frontal region and small callous body with smallbleeding component and mass effect. Patient was prescribed dilantin,suprabion, pharmaton, aerial, lexotanil, and nonie juice. Patient wasalso self medicating with Arcalion until ordered to stop by hisphysician. Approximately one week after the last convulsive crisis, thepatient starts oral treatment with Formulation 1 at a rate of 20 drops aday the first day and then increasing the amount to 120 drops a day bythe fifth day. Two weeks after the last convulsive crisis the patientwas administered 2 cc of Formulation 1 diluted in 500 cc ofphysiologically acceptable solution, intravenously through the left arm.The administration produced severe itching and was stopped. A secondattempt the following week to administer Formulation 1 intravenously wasalso stopped due to severe itching. Formulation 1 was continued orallyat a rate of 120 drops a day. The following week, a subclavian catheterwas installed and the patient was administered 2 cc of Formulation 1 in500 cc of glucose solution three times a day. The catheter wasmaintained in place for 45 days and the dosing regimen maintained withno signs of infection or signs of reaction to Formulation 1. Followingthe administration of Formulation 1, the patient was taken off all othermedications. His convulsions disappeared and his headaches reducedsignificantly in frequency and severity. The patient's appetite returnedand he was able to sleep. His energy level returned to normal. One yearfollowing administration of treatment with Formulation 1, patientcontinues to take Formulation 1 orally every day and has no clinicalmanifestations of the tumor. The last MRI taken 9 months after treatmentwith Formulation 1 shows the tumor to have reduced by 90%. At the filingof this application, the patient continues to take Formulation 1 orallyand remains in good health, with no increase in tumor size.

EXAMPLE 22 Ovarian Cancer

A female age 37 was diagnosed with terminal ovarian cancer. A CAT scanshowed a lesion in the pelvic region of 110×110 mm. Upon undergoinglaparotomy, the surgeon identified a mass which spanned from the uterusto the appendix to the rectum. The tumoral mass completely covered theovary. The surgeon was unable to locate the primary cite of the tumorand did not take a biopsy given the advanced stage of the disease.Patient was given 2 weeks to one month to live. Post surgery, patientwas prescribed analgesics for the constant pain. The patient could noteat solid food and was too weak to walk. Chemotherapy and radiotherapywere considered hopeless but nevertheless offered to the patient, whodeclined to undergo either treatment. Approximately two weeks aftersurgery, patient initiated oral treatment with Formulation 1 at a doseof 40 drops per day increasing to 120 drops per day over the course ofone month, at which point patient is eating solid food. One month afterinitiating treatment, tests confirm the presence of endometrial cancer.By six weeks following treatment, patient shows no signs of abdominalswelling, and her blood work is returning to normal, patient resumeswalking and normal menstruation. FIG. 3A is an ultrasound conducted fourmonths after treatment showing a normal sized left ovary of 34×29 mm andan enlarged right ovary of 36×30 mm due to a solid tumor of 50×46 mm. Atransvaginal ultrasound administered six months following the initiationof treatment with Formulation 1 shows a normal left ovary (34×29 mm) anda slightly enlarged right ovary (31×47.6) with a solid tumor containedwithin the ovary. Ten months after initiating treatment with Formulation1 both ovaries are normal size with no tumor visible. FIG. 3B shows theright ovary now 29×30.1 mm in size. One year after initiating treatmentwith Formulation 1, patient leads a normal life while continuing to takeFormulation 1 orally at a dose of 100 drops per day. Patient received noother treatment for her cancer.

EXAMPLE 23 Prostate Cancer

Male patient, age 64, suffered from frequent episodes of nighttimeurination. Medical examination showed his PSA levels to be 33.49 ng/mland rectal examination indicated a large prostate tumor with metastasis.Patient was very depressed. A second opinion which included a biopsy andechogram confirmed an aggressive carcinoma grade 9/10. An abdominalpelvic cat scan performed one week later showed calcification of thekidneys. Liver and spleen were normal size, uniform density and no focalalteration, incidentally a LOS (lesion of occupying space) ofapproximately 3 cm in diameter is shown at the right suprarenal level,represented by a low density nodular area. The left suprarenal area isnormal. In the pelvis the prostate was observed to be 5 cm in diameter,a noticeable increase in size. Thickening of the back wall of thebladder was also observed and the prostate was exerting pressure on thebladder preventing expansion and increasing the frequency of urination.These findings suggested the presence of a neo proliferation. There areno lymphatic nodes increased in size in the pelvic compartments.Diverticulitis was also observed in the sigmoid colon. Following the CATscan, patient initiated hormone treatment with Eleuxin tablets ever 8hours and Zoladex one vial a month. The following week the patientunderwent a transuretral resection of prostate.

Three weeks after the initial diagnosis, the patient underwent a bonescan. The results of the bone scan are shown in FIG. 4. Metastasis tothe bone, indicated by dark spots, are seen in the right scapula, leftsacroilliac, L1 vertebra and in the ribs. At this time the patientinitiated treatment with Formulation 1 at a dosage of 18 drops, 3 timesa day, increasing 3 drops a day to reach 150 drops a day total by theend of 30 days. The patient continues to take 150 drops a day for twomonths and then reduced the dosage to 140 drops per day. The patientcontinues to take an average of 140 drops a day and continues to takeprescribed doses of hormones.

Nine months post diagnosis of the tumor, the patient is normal with noabnormalities when palpated abdominally. A genital evaluation identifiedno pathological findings, and rectal exam identified a firm glandwithout well defined contours. Subject's PSA level at time of exam was2.74 ng/ml. FIG. 5 is a bone scan taken 8 months after the originaldiagnosis and shows no sign of metastasis.

EXAMPLE 24 Adenocarcinoma of Right Parotid Gland

Female patient age 50 was diagnosed with an adenocarcinoma of the rightparotid by examination confirmed as a 3.1 cm×1.7 cm×1.5 cm tumor throughechogram and MRI. Surgery was performed approximately 7 months postdiagnosis and a 3 cm tumor was extracted. The tumor returned at eightmonths with metastasis to the lymph nodes and the patient was treatedwith 25 sessions of radiotherapy over the following 8 months duringwhich the tumor regressed. One year post diagnosis, a renal echogram wasperformed identifying a hydronephrosis and left kidney litaisis. Thirtyfour months following the original diagnosis, a Neoplastic Right ParotidGland is again identified through MRI. Two months later the patient hasan abdomen and pelvic ultrasound test, and the conclusions were:

-   -   1) Right Litiasis Renal Obstructive.    -   2) Renal Hydronephrosis IV/IV    -   3) Left Liatisasis non obstructive    -   4) Left Kidney of irregular shape, probably related to        infectious process.

Patient decides not to undergo any further conventional therapy.

Approximately thirty-eight months following the initial diagnosis, thepatient presents a painful, visible tumor of 7 cm of diameter withinfiltration to the ear and pre auricular area. A Q-Tip cannot beintroduced into the ear canal. The left side of the patient's facesuffered paralysis caused by the earlier radiation therapy and thepatient had insomnia and cephalea. At this time the patient initiatedoral treatment with Formulation 1 at an initial dose of 30 drops a day,increasing by 6 drops each day until reaching a maximum of 120drops/day. Within one week the patient is taking 70 drops a day and isexperiencing needle like sensations in the area of the tumor and thather head feels lighter. The attending physician observes the tumor to bevisibly decreasing in size. One area of the tumor is squamous, whenbefore is was plain. The following week the patient returned forobservation complaining of dizziness and nausea. One month afterinitiating treatment the patient experienced headaches and lethargy butcontinued taking Formulation 1. Six weeks following treatment thepatient returned for observation at which point the tumor is bleeding,but is noticeably softer, darker and smaller. By this time the dizzinessand headaches have stopped and the patient feels well. The tumorcontinued to bleed and shrink until at two months after startingtreatment a finger can be introduced in the ear.

By ten weeks the tumor shrunk further and shows necrosis until it brokeinside the ear. The patient experienced bleeding through the mouth andear. By twelve weeks following initialization of treatment, the tumorsize is approximately 4 cm. Eighteen weeks after initiation of therapywith Formulation 1 the tumor has shrunk to 3 cm. The patient continuesto take formulation 1.

EXAMPLE 25 Colon Cancer

Male patient, age 38, was diagnosed with adenocarcinoma of the rectum.Diagnosis followed patients suffering rectal bleeding, post-coital pain,loss of weight, changes in intestinal habits, and mid abdominal pain. 5months after manifestation of symptoms, a Gastronterologist whoidentified a rectal mass and performed a colonoscopy and biopsy, withlow anterior resection of the mass, evaluated subject. Subject pathologyon the biopsy shows a T3-N1 Adenocarcinoma of the rectum with negativemargins and one positive lymph node. Surgery was performed 7 monthsafter initial diagnosis and the patient immediately underwentRadiotherapy (3960 cGy) for six months along with concurrentchemotherapy of 28 cycles of 5-FU and Leucovorin. The patient's CEAlevel (carcinoembriogenic antigen) was 0.7. at the time of initialdiagnosis. Fourteen months following the initial diagnosis, anothercolonoscopy was performed revealing a small ulcerous lesion in theanastomosis line of the adrenal gland. The biopsy revealed smallfragments of poorly differentiated adenocarcinoma. Because recurrentcancer was identified, the patient underwent a CT scan of the abdomenand pelvis and chest, along with x-ray and ultrasound. Tests failed toshow any lung or liver metastasis. The patient could feel a nodularthickening of the rectum. At this time the patient was examined at M.D.Anderson Cancer Center and an additional 1.5 cm tumor in the lymph nodeidentified.

The patient declined further radiotherapy, chemotherapy or furthersurgery. At seventeen months post diagnosis, the patient initiated oraltreatment with Formulation 1 at an initial dose of 15 drops 3 times aday, increasing at a rate of 3 drops a day. The following week asubclavian catheter was installed and the patient began intravenousadministration of Formulation 13 cc of 2 times a day (total 6 cc a day).While undergoing IV administration, patient continued to takeFormulation 1 orally, up to 90 drops a day. During the second week oftreatment with Formulation 1, the patient administered Formulation 1rectally, diluted in 100 cc of saline for total of 15 continuous daysusing a rubber bulb. A total of 120 cc was administered via thesubclavian catheter over 20 days at a dose of 6 cc a day. The patientcontinued taking Formulation 1 orally at about 90 drops a day afterremoval of the catheter.

Nineteen months post diagnosis, the patient reported that he could notfeel the anal tumor; he felt in good physical condition, had resumedexercising and had regained his appetite.

20 months post diagnosis, a biopsy shows an adenocarcinoma moderatelydifferentiated with ulceration and necropsies. A colonoscopy showsanastomosis approximately 5 cm from the anal exit, with 2 ulcerousareas. Multiple biopsies were taken and pictures were given to thepatient. The attending physician was unable to find any tumor. There isno report of the lymph node discovered at MD Anderson. The onlymedication the patient has taken since his visit to MD Anderson isFormulation 1.

EXAMPLE 26 Extended Use Of Subclavial Ports

A 10 year old male patient suffering from cancer of the larynx had anexternal subclavian catheter installed. 3 cc of Formulation 1 diluted inphysiological solution was administered twice a day for 95 days. At thetime treatment with Formulation 1 was initiated, patient's esophagus wasobstructed and patient could not eat. Patient was anemic with ahemoglobin level of 9. Following treatment the tumor shrank and thepatient was able to eat normally. Further, the patient's hemoglobinlevel rose to 12. The catheter was in place for 95 days without any signof infection.

EXAMPLE 27 Hypertension

A male patient aged 46 having hypertension since age 18 was treated withFormulation 1. Patient's normal blood pressure without any medicationwas 180/110 which caused patient severe headaches. Patient's bloodpressure was stabilized at 150/90 through the administration of bothActbril and Atenolol twice daily for four years prior to beginningtreatment with Formulation 1. Patient discontinued Actbril and Atenololand immediately began taking 20 drops of Formulation 1 diluted in 250 mlof water twice a day. Patient's blood pressure has remained stable at150/90 for more than 180 days following discontinuing Actbril andAtenolol. Prior to taking Formulation 1, patient experienced immediateelevation of blood pressure and headaches when discontinuing theactbril® and atenolol. Patient experienced no side effects of any kindfrom taking Formulation 1. Patient has only taken Formulation 1 tocontrol his blood pressure for a period of six months.

EXAMPLE 28 Hypertension

An overweight 40 year old male patient with high blood pressure of180/110 was administered Formulation 1 orally 40 drops per day. After 5days, the patient's blood pressure stabilized at 140/90. Patient took noother medication.

EXAMPLE 29 USP51 Preservative Challenge Test

USP51 of the US Pharmacopoeia. It is a standard test that permits todetermine if a medication requires of the presence of a preservative forits preservation, stability and packaging. The tests were carried out inthe an independent testing facility located in Boston. Tests wereperformed at the following dilutions of Formulation 1:1:100, 1:250,1:500 and 1:1000 in cuts of 7, 14 and 28 days for each dilution in thefollowing micro-organisms: S. Aureus, E. Coli, Ps. Aeruginosa, C.Albicans, and A. Niger. Table 8 show similar results of the test at thedifferent dilutions of Formulation 1, and its capacity to inhibit thegrowth of different micro organisms (i.e. Bacteria, Virus and Fungus).TABLE 8 USP51 Preservative Challenge Test with Formulation 1 Dilutions:1:100; 1:250; 1:500; 1:1000 Day 7 Day 14 Day 28 Initial CFU/ml CFU/mlCFU/ml Test Organism Inoculum (% Red) (% Red) (% Red) S. Aureus 3.3 ×10⁵ <10 <10 <10 (>99.99%) (>99.99%) (>99.99%) E. Coli 3.9 × 10⁵ <10 <10<10 (>99.99%) (>99.99%) (>99.99%) Ps. Aeruginosa 2.7 × 10⁵ <10 <10 <10(>99.99%) (>99.99%) (>99.99%) C. Albicans 2.0 × 10⁵ <10 <10 <10(>99.99%) (>99.99%) (>99.99%) A. Niger 3.1 × 10⁵ <10 <10 <10 (>99.99%)(>99.99%) (>99.99%)

Conclusion: Formulation 1 meets the requirements of the USP51 forcategory 1A Products (Injectable Products).

The present invention has been set forth in the form of severalpreferred embodiments. It is nevertheless understood that modificationsto the uses of the acid solutions disclosed herein may be made by thoseskilled in the art without departing from the scope and spirit of thepresent invention. Moreover, such modifications are considered to bewithin the purview of the appended claims.

1. A method of disinfecting comprising the administration or applicationof a composition comprising a mixture of three strong acids and threeweak acids.
 2. The method of claim 1 wherein at least one (1) of theweak acids is hydrofluoric acid.
 3. The method of claim 1 wherein theacids are selected from the group consisting of sulfuric, hydrochloric,oxalic, phosphoric, citric and hydrofluoric acids.
 4. The method ofclaim 1 wherein the acids are present in the following concentrations byweight: HCl 3-25% H₂C₂O₄ 0.1-10%   H₃PO₄ 3-10% HF 1-30%


5. The composition of claim 1 wherein the acids are present in thefollowing concentrations by weight: HCl  5-15% H₂C₂O₄ 0.15-2%   H₃PO₄2-7% HF 2-7%


6. The composition of claim 1 wherein the acids are present in thefollowing approximate concentrations by weight: HCl  11% H₂C₂O₄ 0.3%H₃PO₄   6% H₂SO₄  16% HF   5% H₈C₆O₇ 0.3%


7. The method of claim 1 wherein the acid composition further comprisesglycerin.
 8. The composition of claim one wherein the composition has apH of below 1 before dilution.
 9. The method of claim 1 whereininfection is reduced or prevented in a circulatory access port.
 10. Themethod of claim 9 wherein the acid composition is administered by meansof the circulatory access port.
 11. The method of claim 9 wherein theacid composition is administered intravenously.
 12. The method of claim9 wherein the circulatory access port is selected from the groupconsisting of: stents, peripheral catheters and central catheters. 13.The method of claim 9 wherein the circulatory access port is asubclavian catheter.
 14. A method of treating infection in a patient inneed thereof comprising the administration of an effective amount of astrong acid buffer comprising a mixture of three strong acids and threeweak acids.
 15. The method of claim 14 wherein at least one (1) of theweak acids is hydrofluoric acid.
 16. The method of claim 14 wherein theacids are selected from the group consisting of sulfuric, hydrochloric,oxalic, phosphoric, citric and hydrofluoric acids.
 17. The method ofclaim 14 wherein the acids are present in the following concentrationsby weight prior to dilution: HCl 3-25% H₂C₂O₄ 0.1-10%   H₃PO₄ 3-10% HF1-30%


18. The method of claim 14 wherein the acids are present in thefollowing concentrations by weight prior to dilution: HCl >5-15% H₂C₂O₄0.15-2%   H₃PO₄ 2-7% HF 2-7%


19. A method of preventing growth of microorganisms in a substancecomprising the addition of the composition of claim 1 to the substance.20. The method of claim 19, wherein the substance comprises a tissueculture.